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. 2022 Dec 1;28(12):2633–2645. doi: 10.1038/s41591-022-02059-9

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Extended Data Fig. 6 — LNA043 binding to the FN1 receptor, integrin α₅β₁, and intracellular signaling e.g. via FAK and AKT phosphorylation induces transcriptional counter-regulation of OA-relevant gene expression. Specifically, a, up-regulation of essential cartilage matrix components PRG4, COL2A1, ACAN, COMP, MATN4, COL9A1 results in cartilage matrix synthesis; b, regulation of genes DKK1, FRZB, WNT16 inhibits WNT signaling, which induces chondrogenesis and cartilage regeneration; c, regulation of genes CHRDL2, GREM1, BMP6 inhibits BMP signaling, which prevents detrimental chondrocyte hypertrophy and mineralization in OA; d, downregulation of OA progression mediators OPN, DNER, OPG as well as FN1 splice variants and FN1, which in the OA environment is cleaved into cartilage degradation-promoting fragments, reduces cartilage degeneration and progression of OA. Transparent symbols depict transcriptomics results, colored symbols in vitro assay-confirmed data.